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Updated: Jul 19, 2025
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Activating Autophagy by Aerobic Exercise in Mice
Published on: February 3, 2017
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Autophagy and Exercise: Current Insights and Future Research Directions
Javier Botella1, Christopher S Shaw2, David J Bishop3
1Metabolic Research Unit, School of Medicine and Institute for Mental and Physical Health and Clinical Translation (IMPACT), Deakin University, Waurn Ponds, Victoria, Australia.
International Journal of Sports Medicine
|August 15, 2023
Summary
Exercise impacts cellular degradation (autophagy) in human muscle. This study compares human and mouse gene expression, identifies new phosphorylation targets, and suggests methods to better understand exercise
Area of Science:
- Cellular Biology
- Exercise Physiology
- Molecular Biology
Background:
- Autophagy, a key cellular degradation process, is influenced by exercise in skeletal muscle.
- Current in vivo methods to measure autophagy flux are limited to animal models, hindering human research.
- Understanding exercise-induced autophagy in humans is crucial for muscle health and performance.
Approach:
- Analyzed gene expression data of autophagy receptors and ATG8 family members in human vs. mouse skeletal muscle.
- Summarized human transcriptomic and phosphoproteomic datasets to identify novel regulatory targets.
- Recommended ex vivo autophagy flux assays for human studies.
Key Points:
- Human and mouse skeletal muscle exhibit distinct gene expression profiles for autophagy regulators.
- Identified novel phosphorylation sites linked to exercise-induced changes in LC3B-II levels.
- Exercise may differentially regulate autophagy receptors and flux in humans.
Conclusions:
- Differences in gene expression may explain varied exercise responses between humans and mice.
- Novel phosphorylation sites offer insights into exercise-mediated autophagy modulation.
- Ex vivo assays are recommended for future human autophagy research.
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